Histopathology of Growth Anomaly Affecting the Coral, Montipora capitata: Implications on Biological Functions and Population Viability

Growth anomalies (GAs) affect the coral, Montipora capitata, at Wai'ōpae, southeast Hawai'i Island. Our histopathological analysis of this disease revealed that the GA tissue undergoes changes which compromise anatomical machinery for biological functions such as defense, feeding, digestion, and reproduction. GA tissue exhibited significant reductions in density of ova (66.1–93.7%), symbiotic dinoflagellates (38.8–67.5%), mesenterial filaments (11.2–29.0%), and nematocytes (28.8–46.0%). Hyperplasia of the basal body wall but no abnormal levels of necrosis and algal or fungal invasion was found in GA tissue. Skeletal density along the basal body wall was significantly reduced in GAs compared to healthy or unaffected sections. The reductions in density of the above histological features in GA tissue were collated with disease severity data to quantify the impact of this disease at the colony and population level. Resulting calculations showed this disease reduces the fecundity of M. capitata colonies at Wai'ōpae by 0.7–49.6%, depending on GA severity, and the overall population fecundity by 2.41±0.29%. In sum, GA in this M. capitata population reduces the coral's critical biological functions and increases susceptibility to erosion, clearly defining itself as a disease and an ecological threat

Empirical Models of Transitions between Coral Reef States: Effects of Region, Protection, and Environmental Change

There has been substantial recent change in coral reef communities. To date, most analyses have focussed on static patterns or changes in single variables such as coral cover. However, little is known about how community-level changes occur at large spatial scales. Here, we develop Markov models of annual changes in coral and macroalgal cover in the Caribbean and Great Barrier Reef (GBR) regions

Mechanisms of Rapid Reactive Oxygen Species Generation in Response to Cytosolic Ca2+ or Zn2+ Loads in Cortical Neurons

Excessive “excitotoxic” accumulation of Ca(2+) and Zn(2+) within neurons contributes to neurodegeneration in pathological conditions including ischemia. Putative early targets of these ions, both of which are linked to increased reactive oxygen species (ROS) generation, are mitochondria and the cytosolic enzyme, NADPH oxidase (NOX). The present study uses primary cortical neuronal cultures to examine respective contributions of mitochondria and NOX to ROS generation in response to Ca(2+) or Zn(2+) loading. Induction of rapid cytosolic accumulation of either Ca(2+) (via NMDA exposure) or Zn(2+) (via Zn(2+)/Pyrithione exposure in 0 Ca(2+)) caused sharp cytosolic rises in these ions, as well as a strong and rapid increase in ROS generation. Inhibition of NOX activation significantly reduced the Ca(2+)-induced ROS production with little effect on the Zn(2+)- triggered ROS generation. Conversely, dissipation of the mitochondrial electrochemical gradient increased the cytosolic Ca(2+) or Zn(2+) rises caused by these exposures, consistent with inhibition of mitochondrial uptake of these ions. However, such disruption of mitochondrial function markedly suppressed the Zn(2+)-triggered ROS, while partially attenuating the Ca(2+)-triggered ROS. Furthermore, block of the mitochondrial Ca(2+) uniporter (MCU), through which Zn(2+) as well as Ca(2+) can enter the mitochondrial matrix, substantially diminished Zn(2+) triggered ROS production, suggesting that the ROS generation occurs specifically in response to Zn(2+) entry into mitochondria. Finally, in the presence of the sulfhydryl-oxidizing agent 2,2'-dithiodipyridine, which impairs Zn(2+) binding to cytosolic metalloproteins, far lower Zn(2+) exposures were able to induce mitochondrial Zn(2+) uptake and consequent ROS generation. Thus, whereas rapid acute accumulation of Zn(2+) and Ca(2+) each can trigger injurious ROS generation, Zn(2+) entry into mitochondria via the MCU may do so with particular potency. This may be of particular relevance to conditions like ischemia in which cytosolic Zn(2+) buffering is impaired due to acidosis and oxidative stress

Early sexual maturation, body composition, and obesity in African-American girls.

OBJECTIVE: To describe associations between sexual maturation and body composition in a sample of African-American girls who were participants in phase 1 pilot interventions of the Girls Health Enrichment Multisite Studies. RESEARCH METHODS AND PROCEDURES: Stature, weight, and waist circumference were measured. Pubic hair and breast development were assessed, and body composition was measured by DXA for 147 African-American girls who were 8 to 10 years of age from three field centers. Participants had BMI \u3e or =25th percentile for age (one site) or BMI \u3e or =50th percentile for age. RESULTS: Girls Health Enrichment Multisite Studies girls had greater BMI, fat mass, and percentage body fat than national norms and relatively earlier initiation of breast development and pubic hair. Increasing stages of breast development, but not stages of pubic hair, were related to increased stature, waist circumference, BMI, lean mass, fat mass, and percentage of body fat. Pubescent girls (breast stage \u3e or = 2) were greater than six times as likely to be classified as at risk of overweight (BMI \u3e or = 85th percentile) and greater than eight times as likely to be classified as overweight (BMI \u3e or = 95th percentile) as prepubescent counterparts. Adjusted odds ratios for advanced breast development [breast stage \u3e or = 2 (8 years) or \u3e or = 3 (9 and 10 years)] were 3.6 for risk of overweight and for overweight compared to girls with average or less than average breast development. DISCUSSION: Sexual maturation is important to consider in understanding the classification of overweight and the development of obesity during adolescence. Breast development and pubic hair development should be considered separately for their associations with growth and body composition

NADPH oxidase (NOX) inhibition attenuates acute Ca²⁺ - but not Zn²⁺-induced ROS production.

<div><p>HEt-loaded cultures were exposed to 100 μM NMDA (30 min) or 300 μM Zn²⁺/pyrithione (5 min) alone (red) or after pre-treatment with and in the presence of apocynin (500 µM), or in glucose-free media supplemented with pyruvate (15 mM) (blue) as described (see Materials and Methods). </p> <p><b>A</b>: Representative images of selected fields of neuronal cultures (“Brightfield”), and pseudocolor images (400x) of HEt fluorescence from these neurons before and 30 min following onset of exposure to NMDA (left) or Zn²⁺/pyrithione (right). The pseudocolor bar shows the 12-bit fluorescence intensity range.</p> <p><b>B</b>: Traces show time course of HEt ∆F, normalized to baseline values (F_x/F₀). Dashed lines show linear extrapolation of baseline. Traces show mean ± SD values from 4 experiments. </p> <p><b>C</b>: Quantification of HEt ∆F changes. Values show F_x/F₀ increases after subtraction of the extrapolated baseline value, 30 min after onset of the exposure. ∆F values each represent means (± SEM) of the 4 experiments; * indicates difference from NMDA alone (p< 0.001) by 2-tailed t test. </p></div

Under conditions of oxidative stress and disrupted Zn²⁺ buffering, lower levels of Zn²⁺ influx result in mitochondrial Zn²⁺ entry and ROS production.

<div><p><b>A</b>: Effect of DTDP on Zn²⁺-triggered ROS generation. HEt-loaded cultures were exposed to 50 μM Zn²⁺/pyrithione alone (red), in the presence of DTDP (100 µM, blue), or with both DTDP and RR (10 µM, black) as indicated. Note that the Zn²⁺/pyrithione exposure only induced ROS generation in the presence of DTDP, and that the ROS production was eliminated by RR. Traces show mean ± SD values from 4 experiments.</p> <p><b>B</b>: Quantification of HEt fluorescence changes. Values show HEt fluorescence changes (F_x/F₀) at the times indicated on the traces shown in A. Values represent means (± SEM) of the 4 experiments; * indicates difference from control condition (p< 0.01) by 2-tailed t test.</p> <p><b>C</b>, <b>D</b>: Disruption of cytosolic Zn²⁺ buffering by DTDP markedly increases cytosolic Zn²⁺ rises and uptake into mitochondria. Fluo-Zin3-loaded cultures were exposed to 1 μM Zn²⁺ with 90 mM K⁺ (“Zn²⁺/high-K⁺”, to trigger a low level of Zn²⁺ influx), to FCCP (1 µM), or to DTDP (100 µM) as indicated. In C, when the cultures were first exposed to Zn²⁺/high-K⁺ there was a very small FluoZin-3 ∆F, and subsequent FCCP exposure, to depolarize the mitochondria and release mitochondrially-sequestered Zn²⁺ into the cytosol, caused only a slight further increase. However, adding DTDP after the FCCP produced a large FluoZin-3 ∆F, suggesting that the Zn²⁺ entering during the Zn²⁺/high-K⁺ exposure had been largely buffered in the cytosol with little entering the mitochondria. In contrast (<b>D</b>), when the cultures were first exposed to DTDP (100 µM), there was a minimal FluoZin-3 ∆F, but when the DTDP exposure was followed by Zn²⁺/high-K⁺, the cytosolic ∆F was dramatically increased, and subsequent FCCP exposure resulted in a marked further ∆F, indicative of Zn²⁺ having accumulated within the mitochondria. Traces show mean ± SD values from 120 neurons from 4 experiments.</p> <p><b>E</b>: 50 μM Zn²⁺/high-K⁺ exposure cause mitochondrial ROS production only in the presence of DTDP. HEt-loaded cultures were exposed to 50 μM Zn²⁺/90 mM K⁺ alone (red) or after pre-treatment with and in the presence of DTDP alone (100 µM, blue) or with RR (10 µM, black) as indicated. Traces represent time course of HEt ∆F, normalized to baseline values (F_x/F₀) and show mean ± SD values from 4 experiments. </p> <p><b>F</b>: Quantification of HEt fluorescence changes. Values show HEt fluorescence changes (F_x/F₀) at the times indicated on the traces shown in E. Values represent means (± SEM) of the 4 experiments; * indicates difference from control condition (p< 0.01) by 2-tailed t test.</p></div